Intra-epithelial palatine nerve endings and their regulation of ciliary activity of frog palate epithelium

Chu, Shaoyan; Kennedy, John R.

doi:10.1007/bf00199257

Cited by 5 publications

(2 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The culture medium was changed every 2 d and 5-21d-old tissue cultures were used for measurements. According to Chu and Kennedy (1994), the muscarinic receptors on the membrane of ciliated cells apparently are not lost during culture, and can be maintained throughout the 3-wk culture period.…”

Section: Tissue Culture Preparationmentioning

confidence: 99%

The Mechanism of Ciliary Stimulation by Acetylcholine

Zagoory

Braiman

Priel

2002

The Journal of General Physiology

102

View full text Add to dashboard Cite

Stimulation of ciliary cells through muscarinic receptors leads to a strong biphasic enhancement of ciliary beat frequency (CBF). The main goal of this work is to delineate the chain of molecular events that lead to the enhancement of CBF induced by acetylcholine (ACh). Here we show that the Ca2+, cGMP, and cAMP signaling pathways are intimately interconnected in the process of cholinergic ciliary stimulation. ACh induces profound time-dependent increase in cGMP and cAMP concentrations mediated by the calcium–calmodulin complex. The initial strong CBF enhancement in response to ACh is mainly governed by PKG and elevated calcium. The second phase of CBF enhancement induced by ACh, a stable moderately elevated CBF, is mainly regulated by PKA in a Ca2+-independent manner. Inhibition of either guanylate cyclase or of PKG partially attenuates the response to ACh of [Ca2+]i, but completely abolishes the response of CBF. Inhibition of PKA moderately attenuates and significantly shortens the responses to ACh of both [Ca2+]i and CBF. In addition, PKA facilitates the elevation in [Ca2+]i and cGMP levels induced by ACh, whereas an unimpeded PKG activity is essential for CBF enhancement mediated by either Ca2+ or PKA.

show abstract

Section: Tissue Culture Preparationmentioning

confidence: 99%

The Mechanism of Ciliary Stimulation by Acetylcholine

Zagoory

Braiman

Priel

2002

The Journal of General Physiology

102

View full text Add to dashboard Cite

show abstract

“…It is composed of stratified mucociliary epithelium and underlying connective tissue that is vascularized and highly innervated (Chu et al 1995). Intra-epithelial nerve endings were observed terminating on secretory basal cells, ciliated cells and goblet cells in outgrowths of palate epithelium placed in tissue culture (Chu and Kennedy, 1994).…”

Section: Introductionmentioning

confidence: 99%

Substance P and acetylcholine are co-localized in the pathway mediating mucociliary activity in Rana pipiens

Hernandez

Ortiz

Rosa

et al. 2007

Comparative Biochemistry and Physiology Part B: Biochemistry an

View full text Add to dashboard Cite

Mucociliary activity is an important clearance mechanism in the respiratory system of air breathing vertebrates. Substance P (SP) and acetylcholine play a key role in the stimulation of the mucociliary transport in the frog palate. In this study, retrograde neuronal tracing was combined with immunocytochemistry for SP and choline acetyl transferase (ChAT) in the trigeminal ganglion and for neurokinin-1 receptor (NK1R) in the palate of Rana pipiens. The cells of origin of the palatine nerve were identified in the trigeminal ganglion using the retrograde tracer Fluorogold (FG). Optimal labeling of FG cells in the trigeminal ganglion was obtained at 96 h of exposure. Immunoflorescent shows that SP and acetylcholine are co-localized in 92% of the cells labeled with FG in the trigeminal ganglion. NK1 receptors were found in the membrane of epithelial and goblet cells of the palate. Ultrastructural study of the palate showed axonal-like endings with vesicles in connection with epithelial and goblet cells. These results further support the concerted action of both neurotransmitters in the regulation of mucociliary activity in the frog palate.

show abstract

The effects of the organophosphorous insecticides Dursban™ and Lorsban™ on the ciliated epithelium of the frog palate In Vitro

Swann

Schultz

Kennedy

1996

Arch. Environ. Contam. Toxicol.

View full text Add to dashboard Cite

The ciliotoxic potential of the organophosphorous insecticides Dursban and Lorsban, their active ingredient, chlorpyrifos, and their carrier ingredients (Blanks) were assessed. Since chlorpyrifos inhibits acetylcholinesterase, the acetylcholine-innervated ciliated epithelial cultures of frog palate were used as the model. All compounds caused a decrease in frequency of ciliary beat overtime. EC50 values followed the same order as the time to inhibition. The orders were Lorsban > Dursban > chlorpyrifos, and Lorsban > Dursban approximately Lorsban Blank > Dursban Blank. Stimulation of ciliary beating occurred immediately after exposure to all compounds, followed by inhibition. Dursban, Lorsban, and both Blanks elicited stimulatory effects in the presence of atropine. Atropine only blocked the initial stimulatory response with chlorpyrifos. In addition to chlorpyrifos, some component(s) of the inert ingredients were initially stimulatory but ultimately inhibitory to ciliary beating in the frog palate model. All compounds caused mitochondrial damage, including swelling, disruption of cristae, and loss of matrix.

show abstract

Intra-epithelial palatine nerve endings and their regulation of ciliary activity of frog palate epithelium

Cited by 5 publications

References 29 publications

The Mechanism of Ciliary Stimulation by Acetylcholine

The Mechanism of Ciliary Stimulation by Acetylcholine

Substance P and acetylcholine are co-localized in the pathway mediating mucociliary activity in Rana pipiens

The effects of the organophosphorous insecticides Dursban™ and Lorsban™ on the ciliated epithelium of the frog palate In Vitro

Contact Info

Product

Resources

About